Whether the normal immune system can prevent or control carcinogenesis, i.e., the development of cancer, is central to mechanisms of homeostasis, surveillance, prevention, and interventive management of neoplastic, mutated, infected, or otherwise altered cells. Naturally occurring lymphocytes, macrophages, and other leukocytes and their secretory products, e.g., lymphokines, interleukins, and other immunologic hormones, are being studied to define their effective anticarcinogenic and tumor cell growth inhibitory activities. Lymphotoxin, one of the few lymphokines with cytotoxic activity can prevent carcinogenesis and inhibit tumor cell growth. Anticarcinogenic action is direct and irreversible and occurs without cytotoxicity. Inhibition of tumor cell growth is primarily reversible but can become irreversible due to increased susceptibility of preneoplastic and neoplastic cells to cytolytic destruction by natural killer cells resulting from lymphotoxin target cell interaction. Lymphotoxin at very high concentrations is also directly cytolytic for tumor cells. The direct acting anticarcinogenic activity of lymphotoxin is more potent than the tumor cell inhibitory activity but by also being able to increase target cell sensitivity to the cytoreductive action of naturally cytotoxic lymphocytes the lymphokine may be an effective homeostatic mechanism for control of carcinogenesis at its later stages of development. Lymphotoxin anticarcinogenic, tumor cell growth inhibitory, and cyto-reductive sensitizing activity co-purify into two glycoprotein classes, lymphotoxin I and lymphotoxin II with differing electrical chages. Lymphotoxin I has an isoelectric pH of 4.6 and 5.0 and lymphotoxin II has isoelectric pH's of 5.0 and 7.1 for hamster and human lymphotoxin, respectively. The anticancer actions of lymphotoxin are distinct from other lymphokines including interleukin I, interleukin 2, macrophage migration inhibitory factor, and interferon. Lymphotoxin alters cell surface conformation, membrane fluidity, and large molecular weight membrane glycoprotein synthesis with changes in the latter correlating directly in time and quantity to lymphotoxin induced establishment of the anticarcinogenic state.